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"Morris, Ian"
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DAMP Molecule S100A9 Acts as a Molecular Pattern to Enhance Inflammation during Influenza A Virus Infection: Role of DDX21-TRIF-TLR4-MyD88 Pathway
Pathogen-associated molecular patterns (PAMPs) trigger host immune response by activating pattern recognition receptors like toll-like receptors (TLRs). However, the mechanism whereby several pathogens, including viruses, activate TLRs via a non-PAMP mechanism is unclear. Endogenous \"inflammatory mediators\" called damage-associated molecular patterns (DAMPs) have been implicated in regulating immune response and inflammation. However, the role of DAMPs in inflammation/immunity during virus infection has not been studied. We have identified a DAMP molecule, S100A9 (also known as Calgranulin B or MRP-14), as an endogenous non-PAMP activator of TLR signaling during influenza A virus (IAV) infection. S100A9 was released from undamaged IAV-infected cells and extracellular S100A9 acted as a critical host-derived molecular pattern to regulate inflammatory response outcome and disease during infection by exaggerating pro-inflammatory response, cell-death and virus pathogenesis. Genetic studies showed that the DDX21-TRIF signaling pathway is required for S100A9 gene expression/production during infection. Furthermore, the inflammatory activity of extracellular S100A9 was mediated by activation of the TLR4-MyD88 pathway. Our studies have thus, underscored the role of a DAMP molecule (i.e. extracellular S100A9) in regulating virus-associated inflammation and uncovered a previously unknown function of the DDX21-TRIF-S100A9-TLR4-MyD88 signaling network in regulating inflammation during infection.
Journal Article
Evolutionary history
Few academic historians take an evolutionary perspective on the past, but this outcome was not inevitable. Leading eighteenth-century intellectuals often took evolutionary perspectives, but particularists largely discredited them in and after the 1780s. By the time Spencer and Darwin revived evolutionism in the 1850s, distinctive historical questions and methods were very well-established. Public intellectuals regularly called for Darwinian history, but almost no academics saw much to gain in it. Most twentieth-century social scientists became generalizers but not evolutionists, while most historians not only refused to engage in generalization of any kind but also criticized divisions of labor in which evolutionists would test theories against data generated by historians. Possibilities remain open for a properly evolutionary history, in which scholars trained as historians but asking evolutionary questions would work alongside those trained as evolutionists but analyzing historical data, but currently, this field's prospects depend too much on individual personalities and even luck.
Journal Article
Why the West rules-for now : the patterns of history and what they reveal about the future
Sometime around 1750, English entrepreneurs unleashed the astounding energies of steam and coal, and the world was forever changed. The emergence of factories, railroads, and gunboats propelled the West's rise to power in the nineteenth century, and the development of computers and nuclear weapons in the twentieth century secured its global supremacy. Now, at the beginning of the twenty-first century, many worry that the emerging economic power of China and India spells the end of the West as a superpower. In order to understand this possibility, we need to look back in time. Why has the West dominated the globe for the past two hundred years, and will its power last? Describing the patterns of human history, the archaeologist and historian Ian Morris offers surprising new answers to both questions. It is not, he reveals, differences of race or culture, or even the strivings of great individuals, that explain Western dominance. It is the effects of geography on the everyday efforts of ordinary people as they deal with crises of resources, disease, migration, and climate. As geography and human ingenuity continue to interact, the world will change in astonishing ways, transforming Western rule in the process. Deeply researched and brilliantly argued, Why the West Rules - for Now spans fifty thousand years of history and offers fresh insights on nearly every page. The book brings together the latest findings across disciplines - from ancient history to neuroscience - not only to explain why the West came to rule the world but also to predict what the future will bring in the next hundred years.
TLR2/MyD88/NF-κB Pathway, Reactive Oxygen Species, Potassium Efflux Activates NLRP3/ASC Inflammasome during Respiratory Syncytial Virus Infection
Human respiratory syncytial virus (RSV) constitute highly pathogenic virus that cause severe respiratory diseases in newborn, children, elderly and immuno-compromised individuals. Airway inflammation is a critical regulator of disease outcome in RSV infected hosts. Although \"controlled\" inflammation is required for virus clearance, aberrant and exaggerated inflammation during RSV infection results in development of inflammatory diseases like pneumonia and bronchiolitis. Interleukin-1β (IL-1β) plays an important role in inflammation by orchestrating the pro-inflammatory response. IL-1β is synthesized as an immature pro-IL-1β form. It is cleaved by activated caspase-1 to yield mature IL-1β that is secreted extracellularly. Activation of caspase-1 is mediated by a multi-protein complex known as the inflammasome. Although RSV infection results in IL-1β release, the mechanism is unknown. Here in, we have characterized the mechanism of IL-1β secretion following RSV infection. Our study revealed that NLRP3/ASC inflammasome activation is crucial for IL-1β production during RSV infection. Further studies illustrated that prior to inflammasome formation; the \"first signal\" constitutes activation of toll-like receptor-2 (TLR2)/MyD88/NF-κB pathway. TLR2/MyD88/NF-κB signaling is required for pro-IL-1β and NLRP3 gene expression during RSV infection. Following expression of these genes, two \"second signals\" are essential for triggering inflammasome activation. Intracellular reactive oxygen species (ROS) and potassium (K(+)) efflux due to stimulation of ATP-sensitive ion channel promote inflammasome activation following RSV infection. Thus, our studies have underscored the requirement of TLR2/MyD88/NF-κB pathway (first signal) and ROS/potassium efflux (second signal) for NLRP3/ASC inflammasome formation, leading to caspase-1 activation and subsequent IL-1β release during RSV infection.
Journal Article
A strongly irreducible affine iterated function system with two invariant measures of maximal dimension
A classical theorem of Hutchinson asserts that if an iterated function system acts on
$\\mathbb {R}^{d}$
by similitudes and satisfies the open set condition then it admits a unique self-similar measure with Hausdorff dimension equal to the dimension of the attractor. In the class of measures on the attractor, which arise as the projections of shift-invariant measures on the coding space, this self-similar measure is the unique measure of maximal dimension. In the context of affine iterated function systems it is known that there may be multiple shift-invariant measures of maximal dimension if the linear parts of the affinities share a common invariant subspace, or more generally if they preserve a finite union of proper subspaces of
$\\mathbb {R}^{d}$
. In this paper we give an example where multiple invariant measures of maximal dimension exist even though the linear parts of the affinities do not preserve a finite union of proper subspaces.
Journal Article
On dense intermingling of exact overlaps and the open set condition
We prove that certain families of homogenous affine iterated function systems in $\\mathbb {R}^{d}$ have the property that the open set condition and the existence of exact overlaps both occur densely in the space of translation parameters. These examples demonstrate that in the theorems of Falconer and Jordan–Pollicott–Simon on the almost sure dimensions of self-affine sets and measures, the set of exceptional translation parameters can be a dense set. The proof combines results from the literature on self-affine tilings of $\\mathbb {R}^{d}$ with an adaptation of a classic argument of Erdős on the singularity of certain Bernoulli convolutions. This result encompasses a one-dimensional example due to Kenyon which arises as a special case.
Journal Article